Skip to main content
PMC home page
NIHPA Author Manuscripts logoLink to NIHPA Author Manuscripts
. Author manuscript; available in PMC: 2011 Aug 1.
Published in final edited form as: J Pers Disord. 2010 Dec;24(6):694–708. doi: 10.1521/pedi.2010.24.6.694

REVISING THE BORDERLINE DIAGNOSIS FOR DSM-V: AN ALTERNATIVE PROPOSAL

John G Gunderson 1
PMCID: PMC3147142  NIHMSID: NIHMS313195  PMID: 21158594

Abstract

The changes in the borderline personality disorder (BPD) diagnosis proposed by the DSM-V personality disorder work group involve radical changes in format (prototype and dimensions) and descriptive characteristics (traits). Changes of this magnitude will create an unwelcome and potentially harmful discontinuity with the definition that has guided BPD research and the development of disorder-specific therapies. This paper offers an alternative proposal that was developed in collaboration with clinical and research leaders. It includes modification of existing criteria, use of a diagnostic algorithm based on phenotypes, and giving BPD a hierarchical relationship vis-à-vis other personality disorders. These changes are incremental, diminish overlap and heterogeneity, sustain clinical and research development, and will improve utilization.

Within a year after borderline personality disorder’s (BPD) coming of age was celebrated by the American Journal of Psychiatry (Kernberg & Michaels, 2009; Oldham, 2009) and the American Psychiatric Association’s Annual Meeting, the DSM-V Personality Disorder Work Group has proposed major changes in the BPD diagnosis (prototypes, traits, and dimensions; see dsm5.org). A thoughtful consideration of such change is timely insofar as changes have been few despite an ever-expanding body of research (Blashfield & Intoccia, 2000; Gunderson, 2009). The BPD syndrome defined in DSM-III, III-R, and IV is frequently criticized for too much overlap with other personality disorders and it’s polythetic algorithm allows too much heterogeneity.

The proposed changes by the DSM-V work group radically alter a definition of BPD that has survived with minimal changes since it entered the DSM system 30 years ago and from which has come a body of knowledge about heritability (Distell et al., 2008; Kendler, Meyers, Torgerson, Neade, & Reichborn-Kjennerud, 2008; Torgerson et al., 2000, 2008), prevalence (Grant et al., 2008; Lenzenweger, Lane, Loranger, & Kessler, 2007; Trull, Jahng, Tomko, Wood, & Sher, in press), developmental antecedents (Cohen, Crawford, Johnson, & Kasen, 2005; Winograd, Cohen, & Chen, 2008; Yen et al., 2002), markers of risk (Crick, Murray-Close, & Woods, 2005; Lyons-Ruth, Melnick, Patrick, & Hobson, 2007), course (Skodol et al., 2004; Zanarini et al., 2008; Zanarini, Frankenbury, Reich, & Fitzmaurice, 2010), and treatment. As to the latter, many empirically-validated psychotherapeutic treatments have been developed while an increasing number of medication studies have been instructive (Lieb, Vollm, Rucker, Timmer, & Stoffers, 2010). Moreover, because in its present form the BPD diagnosis has been validated (Gunderson 2009; New, Triebwasser, & Charney, 2008), and because it has become a recognizable clinical entity that informs the hopes and the therapies for patients who would otherwise be undiagnosable, changes in its definition should proceed with caution and only with sound empirical justification.

The proposal offered here is guided by the conservative standards established in DSM-IV: all changes were required to have an empirical rationale, meaning reliably assessable with demonstrated diagnostic efficacy. In addition, changes proposed here will be guided by considerations of clinical utility (i.e., familiarity, coverage for patients who benefit from BPD’s treatments), continuity with past research, and the potential to diminish problems with underutilization, oversight, and stigma.

BPD’s CRITERIA

The current definition of the BPD diagnosis was largely developed in the late 1970s. It developed as a result of the first empirical study (Grinker, Werble, & Drye, 1968), a swelling clinical interest (Kernberg, 1968; Masterson, 1972), a review of relevant literature (Gunderson & Singer, 1975), and the development of a reliable diagnostic method (Gunderson & Kolb, 1978, 1981). The latter provided a method to reliably distinguish BPD patients from those with schizophrenia or depression, established a cut-point/threshold for making the diagnosis, and identified seven characteristics that were highly discriminating (Gunderson & Kolb, 1978). These seven characteristics, with some modifications, and with the addition of an eighth criterion for identity disturbance (Spitzer, Endicott, & Gibbon, 1979), became the criteria for BPD adopted in DSM-III in 1980. Since then the only substantial change has been the addition into DSM-IV of a ninth criterion psychotic-like experiences in 1994.

The current criteria have all been validated, have an established research legacy, and have generally proven clinically valuable. All have been examined for their relative specificity, sensitivity, and predictive power (Clarkin, Widiger, Frances, Hurt, & Gilmore, 1983; Grilo et al., 2007; Gunderson, Zanarini, & Kisiel, 1996). The only criterion to be added since 1980, i.e., psychotic-like experiences, required significant empirical justification and demonstrating that it did not increase prevalence (Sternbach, Judd, & Sabo, 1992; Gunderson et al., 1996). These criteria have been the basis for research validating BPD as a diagnostic entity (Gunderson, 2009; New et al., 2008; Paris, 2007).

Since DSM-IV, many new studies have examined BPD phenomenology. Table 1 incorporates findings from these studies that appear to add to both the specificity and clinical valence of the current criteria.

TABLE 1.

Proposed Changes in DSM-IV BPD Criteria: Four Sectors

Open in a new tab

[Criterion Rating Rate the extent to which each criterion is descriptive of the patient (adapted from Shedler & Westen, 2004; Trull et al., in press):

0 = Not

1 = Mild

2 = Moderate

3 = Strong]

The proposed changes in interpersonal criteria (criteria 2 & 3) derive from the growing body of research on attachment and social psychology. They can be expected to add specificity and bridge the criteria to therapies such as Mentalization Based Treatment (MBT; Bateman & Fonagy, 2004; Fonagy, Target, & Gergely, 2000) and Schema Focused Therapy (SFT; Young, Klosko, & Weishaar, 2003). The proposed changes in affective (emotion) criteria (4 & 5) derive from a growing body of research including neurophysiology and experience-sampling. While the DSM III and IV criterion for affective instability (criterion 4) has been sensitive, it has not been specific (Grilo, Becker, Anez, & McGlashan, 2009; Gunderson, Zanarini, & Kisiel, 1991). The changes proposed for this criterion capture the pervasive negativity of mood alongside specific types of instability. It will provide valuable help in distinguishing BPD from bipolar disorder—where “affective instability” has become a passport for diagnosing bipolar disorder (Zimmerman, Ruggera, Chelminski, & Young, 2010). The use of Negative links it to neuroticism and the use of Emotionality links this criterion to Dialectical Behavior Therapy (DBT) and the construct of emotional dysregulation (Linehan, 1993). The proposed change in criteria 8 (i.e., sense of badness) reflects a widely-recognized and empirically-validated aspect of the borderline patients’ sense of self and will add specificity. The change proposed for criteria 9 returns to the historically-valued observation that borderline patients lack a sense of reality (Frosch, 1970); that is, experiences of disconnection or dissociation, thereby shifting it from an episodic symptom into more of a personological construct (Waller & Ross, 1997).

The final change (also used in the DSM-V prototype and trail schemes), would be to move ratings of criteria from an absent-present dichotomy to a more dimensional four-point scale from Not to Mild to Moderate to Strong (see Table 1). This change has conceptual and statistical advantages over the current system.

The magnitude of the proposed changes in the content of the criteria is greater than those approved in DSM-III-R or DSM-IV, but are modest compared to the changes proposed by the DSM-V committee. All of the changes proposed here have been empirically shown to discriminate BPD from other disorders. None of these changes depart from the basic clinical construct each criterion was designed to represent. Still, it is unclear whether the newly added components might better be separated into their own independent criterias, e.g., alternating between overinvolved and withdrawal or chronic dysphoria.

BPD’s DIAGNOSTIC ALGORITHM

DSM-IV uses a polythetic system (adding the number of criteria without weighting) with the diagnosis of BPD requiring five (or more) of the nine criteria. This means that there are 256 different combinations of criteria from which the diagnosis might be established. Two patients getting this diagnosis might overlap on as few as only one criterion. This allows too much heterogeneity in the people who can receive the diagnosis. It contrasts with the relative ease with which the diagnosis can usually be established—due to differences in the clinical weighting of criteria. One study showed that the combination of criterion 7 (self-injurious behaviors) and criterion 1 (intense unstable relations) were usually sufficient to predict the diagnosis (Grilo et al., 2007).

It would reflect what is known about BPD’s latent structure and diminish the disorder’s heterogeneity to subdivide the criteria set into four component sectors and base the scoring algorithm on them. Three components have been solidly established as phenotypes (signifying significant heritability) based on the results of factor analyses (Blais, Hilsenroth, & Castlebury, 1997; Clarkin, Hull, & Hurt, 1993; Hurt, Hyler, Frances, Clarkin, & Brent, 1989; Sanislow et al., 2002; Skodol et al., 2002), family studies (Gunderson et al., unpublished; Silverman et al., 1991; Zanarini et al., 2004) and increasing evidence of their endophenotypes, that is, neurobiological correlates (King-Casas et al., 2008; Koenigsberg et al., 2009; Siever, Torgerson, Gunderson, Livesley, & Kendler, 2002; Stanley & Siever, 2010). Factor analytic studies generally divide BPD psychopathology into three sector or phenotypes: Interpersonal Hypersensitivity (criteria 1, 2, and 3), Affective/Emotional Dysregulation (criteria 4, 5), and Behavioral Dyscontrol (criteria 6, 7). Major clinical theories (and the effective therapies that are based on them) have proposed that the Interpersonal (Adler, 1986; Bateman & Fonagy, 2004; Benjamin, 1993; Gunderson, 2007) or the Affective/Emotional (Linehan, 1993; Livesley, Jackson, & Schroeder, 1992) phenotypes are the core component. These are the phenotypes that are also more stable over time (Zanarini et al., 2007). While the Behavioral phenotype is not central to any major clinical theory or therapy, it gains significance by virtue of its link to a biogenetic dimension called impulsive/aggression (Coccaro, Bergman, & McLean, 1993, 1997), its power to explain co-aggregation patterns (White, Gunderson, Zanarini, & Hudson, 2003), and the genetic link of BPD to antisocial personality disorder (ASPD; Torgersen et al., 2008).

Kernberg’s enduring theoretical and therapeutic contributions were responsible for initially introducing the identity disturbance criterion (criterion 8; Spitzer et al., 1979). This criterion has proved to be reasonably efficient (Gunderson et al., 1996), but not very longitudinally persistent (Zanarini et al., 2007). The proposed change (see Table 1) should add to its specificity. The ninth criterion becomes a conceptual partner to criterion 8, and more trait-like by shifting its emphasis to recurring dissociative splits (perceiving oneself or the outer world as unreal; consistent with Akhtar & Thomson, 1982; Kernberg, 1975; Korzekwa, Dell, Links, Thabanc, & Fougere, 2010) (see Table 1). Combined they yield a fourth sector that might be identifiable as Disturbed Self. Such a sector has conceptual coherence, honors the contributions from Kernberg and object relations theory, and links the criteria set to Transference Focused Psychotherapy (TFP; Clarkin, Yeomans, & Kernberg, 2006). This sector also recognizes the role of dissociation that serves as a defensive flight from either aloneness (Gunderson, 1984) or feelings (Linehan, 1993). The potential centrality of this sector is reflected in the prominence it attained in the proposed DSM-V definition for all PDs (see dsm5.org) and specifically in the proposed BPD prototype (see dsm5.org).

To be diagnosed BPD, the proposed changes would require that a person continue to have ≥5 criteria, but require at least one criterion from at least three sectors. Several empirical questions remain; should the four phenotypes be weighed differently (as is currently done with MDD and PTSD)? Should the diagnostic threshold require psychopathology in 3 or 4 sectors? Three would be more inclusive (increased sensitivity) and might be preferred within the psychotherapeutic community; and four (increased specificity) would probably be preferred by researchers, who value narrower homogeneous samples. However these questions are answered, the proposed algorithm moves the diagnosis away from observable symptoms towards underlying phenotypes (and endophenotypes) which lie closer to the genetic template (Gottesman & Gould, 2003). Nor does the proposed shift from criteria to phenotype prematurely bias the diagnosis towards any of the competing models about which sector should be considered primary. Finally, it offers a relatively discrete way to identify a diagnostic threshold—lacking altogether in the proposed schemes of DSM-V. [This model for the BPD diagnosis is validated by family study results which show that when the phenotypes are used to establish the BPD diagnosis, it is more familial than when diagnosed with the DSM-IV criteria system (Zanarini et al presented American Psychiatric Association, 2009).]

BPD’s PLACE IN THE DSM CLASSIFICATION SYSTEM

BPD does not easily lend itself to the changes (dimensions, trait profiles, and prototypes) being proposed for it in DSM-V (see dsm5.org). Many other personality disorders lend themselves to dimensional schemes because they reflect traits that extend seamlessly into normality (e.g., dependency or avoidance). Although one taxometric study indicated that BPD is more dimensionally-related to normality than categorically separate (Rothschild, Cleland, Haslam, & Zimmerman, 2003), BPD’s diverse components (noted above), each of which might be dimensionalized, cannot easily be blended into any single dimension. Several factor analytic studies show that the disorder is best modeled as a single factor (Fossati et al., 1999; Clifton & Pilkonis, 2007), but we can’t yet identify what that core factor is. Nor does BPD fit into the quantitatively-developed architecture of personality traits: it relates equally to both internalizing and externalizing (Depue & Lenzenweger, 2005), and to both antagonism and negative emotionality— thus being “interstitial” (Krueger & Eaton, in press). The traits definition proposed for BPD (see dsm5.org) is not empirically-based and is completely divorced from clinical concepts and literature. Prototypes have been shown to have advantages for clinicians in identification of personality disorders (Shedler & Westen, 2004), but BPD already has a validated and clinically-useful definition for which a format change of such magnitude cannot be easily justified. The prototype model returns us to the problems of DSM I and II and sets BPD and other PDs apart from all other medical diagnoses. Moreover, the specific prototype proposed for BPD in DSM-V (see dsm5.org) is relatively discursive, theory-driven (the concepts of self and identity are central), has unknown and probably difficult-to-attain reliability, and is not tightly anchored to research citations or to databases from either DSM-IV or the Shedler-Westen Assessment Procedure (SWAP; Westen & Shedler, 1999).

Genetically, Kendler et al. (2008) have indicated that BPD shares some of the genetic template common to personality disorders but much of its genetic vulnerability is not. (Moreover, it shares just as much with the genetic template for the axis I sector of psychopathology; Kendler et al., in press.) [The idea of some still unidentified and specific core to BPD psychopathology is further supported by preliminary results of the Family Study in which the disorder appears to be more familial than are its phenotypes (Gunderson et al., 2010).] Such research findings would seem to confirm Paris’s (2007) earlier conclusion that BPD appears to be “more than the sum of its parts” (p. 968).

As a clinical entity, BPD does not fit comfortably alongside the other personality disorders. Certainly it is the personality disorder that is the most dystonic (Paris, 2007) and most prevalent in clinical settings. The intensity and duration of treatment utilization by BPD patients and their severe social dysfunction (and derivative costs) underscore the disorder’s extraordinary public health significance. The psychotherapeutic office-practice community is likely to use personality diagnoses as a primary way to organize their treatment, but in other settings the personality disorders are likely to be considered as either: (1) adjunctive to axis I disorders (i.e., they may help clinicians anticipate resistances), or (2) latent vulnerabilities to presumably primary Axis I disorder(s). Both conceptualizations are an argument to keep the PDs in a separate and subordinate relationship to Axis I disorders in DSM-V, as has been the case since Axis II was introduce in DSM-III. But neither of these models reflect BPD’s relationship to axis I. The Collaborative Longitudinal Personality Disorders Study (CLPS) has shown that BPD has a negative effect on the course of substance use disorders (Walter et al., 2009), major depression (Gunderson et al., 2004, 2008; Morey et al., 2010), bipolar disorder (Gunderson et al., 2006) and panic disorder (Gunderson et al., unpublished), but these disorders had no, or relatively little, reciprocal effect on the course of BPD. Thus, even in the presence of major Axis I comorbidity, BPD should often be a primary target for treatment. Only ASPD might claim to have a comparably negative effect on the prognosis for Axis I disorders (Gunderson, 1984; Kernberg, 1968; Reich, 1988; Woody, McLellan, Luborsky, & O’Brien, 1985). Finally, only BPD can claim to have empirically validated disorder-specific therapies that hasten the remission of its symptoms (criteria) and decrease treatment utilization.

Because the BPD diagnosis is greatly underutilized (Zimmerman et al., 1999, 2010), and because most clinicians lack training in treating BPD and do not like working with them (Shanks, Pfohl, Blum, & Black, in press); changes in DSM-V should encourage its use by making the diagnosis more visible and accessible. In DSM-III and IV, placing BPD under the parent class of PDs may have encouraged excessive use of the residual category, PDNOS (Blashfield & Intoccia, 2000). Though in the current DSM-V proposal all the personality disorders are placed in Axis I, BPD remains buried behind an even more complex and lengthy filter that is proposed to be classified as having a personality disorder (see Shedler et al.,, 2010). Rather than encouraging and stimulating more appropriate utilization of the BPD diagnosis, the DSM-V work group’s proposed revisions may de facto defeat the hope of making the BPD diagnosis harder to overlook by placing it on Axis I (Gunderson, 2009; New et al., 2008; Paris, 2007). BPD needs to be featured as a primary target for treatment. Such prominence will serve as a stimulus for training programs to include this disorder in their curricula, help support fair reimbursement policies by third party payors, and help this diagnosis gain parity.

The reasons for giving BPD a hierarchical relationship to other personality disorders are impressive, but how to do this is unclear. If it were to move to the mood disorders, it would benefit utilization and decrease stigma. However, this change would magnify the current overuse of medication and underutilization and training in psychosocial interventions. Moreover, it would bury the role of interpersonal hypersensitivity. If it was identified as an Impulse Control disorder, this too might help utilization and stigma, but would not reflect any of the major theories of etiology or therapy. It might be least prejudicial for BPD to be considered as an anxiety disorder. This could be justified conceptually, but it is not reflected well in the criteria. Perhaps the best option is to have it stand alone (or with ASPD) on Axis I with all other PDs remaining on Axis II.

CONCLUSIONS

The changes in BPD’s diagnosis proposed here are offered with recognition that the proposed move towards dimensions and a scientific personology endorsed by Drs. Kupfer and Regier (Regier, Narrow, Kuhl, & Kupfer, 2009) should one day supersede and reorganize our classification. At the present, however, as per the letter from Drs. Spitzer and Frances (letter to Board of Trustees, American Psychiatric Association, July 6, 2009), a huge gap remains between the still preliminary development of that scientific nosology and its application to clinical practice.

Changes in the BPD criteria and their ratings that are proposed integrate levels of severity and have both an empirical and conceptual rationale that do not radically effect their meaning. The changes should make the criteria more specific, and thereby diminish both BPD’s overlaps and its heterogeneity. The change proposed for the diagnostic algorithm moves from number of criteria to number of phenotypes; i.e., Interpersonal Hypersensitivity, Affective/Emotional Dysregulation, Behavioral Dyscontrol, and Disturbed Self. This diminishes heterogeneity, mirrors knowledge about BPD’s underlying structure, and retains continuity with prior research. The specific algorithm for establishing the BPD diagnosis will require empirical exploration. The final change proposed, that is, assigning BPD a hierarchical priority to other personality disorders (with the exception, perhaps, of ASPD) will unquestionably improve utilization, awareness, and stimulate training and research.

This proposal has developed with the input of many researchers and clinicians who have made contributions to BPD (see Appendix). Each may find aspects to disagree with, but all are seriously dissatisfied with the DSM-V proposal and all support the mode from which this proposal evolved: transparent, interactive, science-based, and having face-value clinical utility to those who treat patients. The proposed changes invite empirical assessments, most significantly how the changes will effect coverage, but they all honor the basic integrity of the current diagnosis, the clinical and research base that has developed from it, and adds impetus to the growing awareness and clinical utility of the borderline diagnosis.

Acknowledgments

This work was supported by National Institute of Mental Health (NIMH), Collaborative Longitudinal Personality Disorders Study (MH400122) and Family Study (MH400130).

APPENDIX

LIST OF SUPPORTERS

Bateman, Anthony, MD

Beck, Aaron T., MD

Black, Donald W., MD

Bohus, Martin, MD

Choi-Kain, Lois W., MD

Clarkin, John F, PhD

First, Michael B., MD

Fonagy, Peter, PhD

Gabbard, Glen O., MD

Goodman, Marianne, MD

Hoffman, Perry D., PhD

Koenigsberg, Harold W., MD

Lenzenweger, Marc F., PhD

Linehan Marsha M., PhD

McGlashan, Thomas H., MD

New, Antonia S., MD

Paris, Joel, MD

Pilkonis, Paul A., PhD

Ronningstam, Elsa F., PhD

Schulz, S. Charles, MD

Silk, Kenneth R., MD

Soloff, Paul H., MD

Stanley, Barbara H., MD

Trull, Timothy J., PhD

Zanarini, Mary C., EdD

REFERENCES

  1. Adler G. Borderline psychopathology and its treatment. New York: Jason Aronson; 1986. [Google Scholar]
  2. Agrawal HR, Gunderson JG, Holmes BM, Lyons-Ruth K. Attachment studies with borderline patients: A review. Harvard Review of Psychiatry. 2004;12:94–104. doi: 10.1080/10673220490447218. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Akhtar S, Thomson JA., Jr Overview: narcissistic personality disorder. American Journal of Psychiatry. 1982;139:12–20. doi: 10.1176/ajp.139.1.12. [DOI] [PubMed] [Google Scholar]
  4. Bateman A, Fonagy P. Psycho therapy for borderline personality disorder—Mentalization-based treatment. Oxford, U.K.: Oxford University Press; 2004. [DOI] [PubMed] [Google Scholar]
  5. Benjamin LS. Interpersonal diagnosis and treatment of personality disorders. New York: Guilford Press; 1993. [Google Scholar]
  6. Bhar SS, Brown GK, Beck AT. Dysfunctional beliefs and psychopathology in borderline personality disorder. Journal of Personality Disorders. 2008;22:165–177. doi: 10.1521/pedi.2008.22.2.165. [DOI] [PubMed] [Google Scholar]
  7. Blais MA, Hilsenroth MJ, Castlebury D. Content validity of the DSM-IV borderline and narcissistic personality disorder criteria sets. Comprehensive Psychiatry. 1997;38:31–37. doi: 10.1016/s0010-440x(97)90050-x. [DOI] [PubMed] [Google Scholar]
  8. Blashfield RK, Intoccia V. Growth of the literature on the topic of personality disorders. American Journal of Psychiatry. 2000;157:472–473. doi: 10.1176/appi.ajp.157.3.472. [DOI] [PubMed] [Google Scholar]
  9. Blum N, St. John D, Pfohl B, Stuart S, McCormick B, Allen J, Arndt S, Black DW. Systems training for emotional predictability and problem solving (STEPPS) for outpatients with borderline personality disorder: A randomized controlled trial and 1-year follow-up. American Journal of Psychiatry. 2008;165:468–478. doi: 10.1176/appi.ajp.2007.07071079. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Butler AC, Brown GK, Beck AT, Grisham JR. Assessment of dysfunctional beliefs in borderline personality disorder. Behavior Research Therapy. 2002;40:1231–1240. doi: 10.1016/s0005-7967(02)00031-1. [DOI] [PubMed] [Google Scholar]
  11. Choi-Kain LW, Hudson J, Zanarini MC, Gunderson JG. Familiality of rejection sensitivity in BPD. Presented at the 163rd American Psychiatric Association; New Orleans, LA. 2010. May, [Google Scholar]
  12. Choi-Kain LW, Fitzmaurice GM, Zanarini MC, Laverdiere O, Gunderson JG. The relationship between self-reported attachment styles, interpersonal dysfunction, and borderline personality disorder. Journal of Nervous and Mental Disease. 2009;197:816–821. doi: 10.1097/NMD.0b013e3181bea56e. [DOI] [PubMed] [Google Scholar]
  13. Clarkin JF, Hull JW, Hurt SW. Factor structure of borderline personality disorder criteria. Journal of Personality Disorders. 1993;7:137–143. [Google Scholar]
  14. Clarkin JF, Widiger TA, Frances A, Hurt SW, Gilmore M. Prototypic typology and the borderline personality disorder. Journal of Abnormal Psychology. 1983;92:263–275. doi: 10.1037//0021-843x.92.3.263. [DOI] [PubMed] [Google Scholar]
  15. Clarkin JF, Yeomans FE, Kernberg OF. Psychotherapy for borderline personality disorder: Focusing on object relations. Washington, DC: American Psychiatric Press; 2006. [Google Scholar]
  16. Clifton A, Pilkonis PA. Evidence for a single latent class of diagnostic and statistical manual of mental disorders borderline personality pathology. Comprehensive Psychiatry. 2007;48:70–78. doi: 10.1016/j.comppsych.2006.07.002. [DOI] [PubMed] [Google Scholar]
  17. Coccaro EF, Bergman CS, McLean GE. Heritability of irritable impulsiveness: A study of twins reared together and apart. Psychiatry Res. 1993;48:229–242. doi: 10.1016/0165-1781(93)90074-q. [DOI] [PubMed] [Google Scholar]
  18. Coccaro EF, Kavoussi RJ. Fluoxetine and impulsive aggressive behavior in personality-disordered subjects. Archives of General Psychiatry. 1997;54:1081–1088. doi: 10.1001/archpsyc.1997.01830240035005. [DOI] [PubMed] [Google Scholar]
  19. Cohen P, Crawford TN, Johnson JG, Kasen S. The children in the community study of developmental course of personality disorder. Journal of Personality Disorders. 2005;19:466–486. doi: 10.1521/pedi.2005.19.5.466. [DOI] [PubMed] [Google Scholar]
  20. Conklin CZ, Westen D. Borderline personality disorder in clinical practice. American Journal of Psychiatry. 2005;162:867–875. doi: 10.1176/appi.ajp.162.5.867. [DOI] [PubMed] [Google Scholar]
  21. Crick NR, Murray-Close D, Woods K. Borderline personality features in childhood: A short-term longitudinal study. Developmental Psychopathology. 2005;17:1051–1070. [PubMed] [Google Scholar]
  22. Depue RA, Lenzenweger MF. A neurobehavioral model of personality disturbance. In: Lenzenweger MF, Clarkin JF, editors. Major theories of personality disorder. 2nd ed. New York: Guilford; 2005. pp. 391–453. [Google Scholar]
  23. Distel MA, Trull TJ, Derom CA, Thiery EW, Grimmer MA, Martin NG, Willemsen G, Boomsma DI. Heritability of borderline personality disorder features is similar across three countries. Psychological Medicine. 2008;38:1219–1229. doi: 10.1017/S0033291707002024. [DOI] [PubMed] [Google Scholar]
  24. Domes G, Czieschnek D, Weidler F, Berger C, Fast K, Herpertz SC. Recognition of facial affect in borderline personality disorder. Journal of Personality Disorders. 2008;22:135–147. doi: 10.1521/pedi.2008.22.2.135. [DOI] [PubMed] [Google Scholar]
  25. Donegan NH, Sanislow CA, Blumberg HP, Fulbright RK, Lacadie C, Skudlarski P, et al. Amygdala hyperreactivity in borderline personality disorder: Implications for emotional dysregulation. Biological Psychiatry. 2003;54:1285–1293. doi: 10.1016/s0006-3223(03)00636-x. [DOI] [PubMed] [Google Scholar]
  26. Drapeau M, Perry JC. The core conflictual relationship themes (CCRT) in borderline personality disorder. Journal of Personality Disorders. 2009;23:425–431. doi: 10.1521/pedi.2009.23.4.425. [DOI] [PubMed] [Google Scholar]
  27. Fonagy P, Target M, Gergely G. Attachment and borderline personality disorder: A theory and some evidence. Psychiatric Clinics of North America. 2000;23:103–122. doi: 10.1016/s0193-953x(05)70146-5. [DOI] [PubMed] [Google Scholar]
  28. Fossati A, Maffei C, Bagnato M, Donati D, Namia C, Novella L. Latent structure analysis of DSM-IV borderline personality disorder criteria. Comprehensive Psychiatry. 1999;40:72–79. doi: 10.1016/s0010-440x(99)90080-9. [DOI] [PubMed] [Google Scholar]
  29. Frosch J. Psychoanalytic considerations of the psychotic character. Journal of American Psychoanalytic Association. 1970;18:24–50. doi: 10.1177/000306517001800102. [DOI] [PubMed] [Google Scholar]
  30. Gottesman II, Gould TD. The endophenotype concept in psychiatry: Etymology and strategic intentions. American Journal of Psychiatry. 2003;160:636–645. doi: 10.1176/appi.ajp.160.4.636. [DOI] [PubMed] [Google Scholar]
  31. Grant BF, Chon P, Goldstein RB, Huang B, Stinson FS, Saha TD, et al. Prevalence, correlates, disability, and comorbidity of DSM-IV borderline personality disorder: Results from the wave 2 national epidemiologic survey on alcohol and related conditions. Journal of Clinical Psychiatry. 2008;69:533–537. doi: 10.4088/jcp.v69n0404. [DOI] [PMC free article] [PubMed] [Google Scholar]
  32. Grilo CM, Becker DF, Anez LM, McGlashan TH. Diagnostic efficiency of DSM-IV criteria for borderline personality disorder: An evaluation in Hispanic men and women with substance use disorders. Journal of Consulting of Clinical Psychology. 2009;72:126–131. doi: 10.1037/0022-006X.72.1.126. [DOI] [PubMed] [Google Scholar]
  33. Grilo CM, Sanislow CA, Skodol AE, Gunderson JG, Stout RI, Bender DS, et al. Longitudinal diagnostic efficiency of DSM-IV criteria for borderline personality disorder: A two-year prospective study. Canadian Journal of Psychiatry. 2007;52:357–362. doi: 10.1177/070674370705200604. [DOI] [PubMed] [Google Scholar]
  34. Grinker R, Werble B, Drye R. The borderline syndrome: A behavioral study of ego functions. New York: Basic Books; 1968. [Google Scholar]
  35. Gunderson JG. Borderline personality disorder. Washington, DC: American Psychiatric Press; 1984. [Google Scholar]
  36. Gunderson JG. Disturbed relationships as a phenotype for borderline personality disorder. American Journal of Psychiatry. 2007;164:1637–1640. doi: 10.1176/appi.ajp.2007.07071125. [DOI] [PubMed] [Google Scholar]
  37. Gunderson JG. Borderline personality disorder: Ontogeny of a diagnosis. American Journal of Psychiatry. 2009;166:530–539. doi: 10.1176/appi.ajp.2009.08121825. [DOI] [PMC free article] [PubMed] [Google Scholar]
  38. Gunderson JG, Kolb JE. Discriminating features of borderline patients. American Journal of Psychiatry. 1978;135:792–796. doi: 10.1176/ajp.135.7.792. [DOI] [PubMed] [Google Scholar]
  39. Gunderson JG, Kolb JE, Austin V. The diagnostic interview for borderline patients. American Journal of Psychiatry. 1981;138:896–903. doi: 10.1176/ajp.138.7.896. [DOI] [PubMed] [Google Scholar]
  40. Gunderson JG, Links P. Borderline personality disorder: A clinical guide. Second Edition. Washington, DC: American Psychiatry Press, Inc.; 2008. [Google Scholar]
  41. Gunderson JG, Morey LC, Stout RL, Skodol AE, Shea MT, McGlashan TH, et al. Major depressive disorder and borderline personality disorder revisited: Longitudinal interactions. Journal of Clinical Psychiatry. 2004;65:1049–1056. doi: 10.4088/jcp.v65n0804. [DOI] [PubMed] [Google Scholar]
  42. Gunderson JG, Singer MT. Defining borderline patients: An overview. American Journal of Psychiatry. 1975;132:1–10. doi: 10.1176/ajp.132.1.1. [DOI] [PubMed] [Google Scholar]
  43. Gunderson JG, Stout RL, Sanislow CA, Shea MT, McGlashan TH, Zanarini MC, et al. New episodes and new onsets of major depression in borderline and other personality disorders. Journal of Affective Disorders. 2008;111:40–45. doi: 10.1016/j.jad.2008.01.026. [DOI] [PMC free article] [PubMed] [Google Scholar]
  44. Gunderson JG, Weinberg I, Kueppen-bender KD, Daversa M, Zanarini MC, Shea MT, et al. Descriptive and longitudinal observations on the relationship of borderline personality disorder (BPD) and bipolar disorders. American Journal of Psychiatry. 2006;163:1173–1178. doi: 10.1176/ajp.2006.163.7.1173. [DOI] [PubMed] [Google Scholar]
  45. Gunderson JG, Zanarini MC, Choi-Kain LW, Hudson J. Familiality of BPD’s Component Phenotypes. Presented at the 163rd Annual Meeting of the American Psychiatric Association; New Orleans, LA. 2010. May, [Google Scholar]
  46. Gunderson J, Zanarini M, Kisiel C. Borderline personality disorder: A review of data on DSM-III-R descriptions. Journal of Personality Disorders. 1991;5:340–352. [Google Scholar]
  47. Gunderson JG, Zanarini MC, Kisiel C. Borderline Personality Disorder, in DSM-IV Source Book, Section IV. Vol. 2. Washington, DC: American Psychiatric Association Press; 1996. pp. 717–733. [Google Scholar]
  48. Hurt SW, Hyler SE, Frances A, Clarkin JF, Brent R. Assessing BPD with self-report, clinical interview, or semistructured interview. American Journal of Psychiatry. 1989;141:1228–1231. doi: 10.1176/ajp.141.10.1228. [DOI] [PubMed] [Google Scholar]
  49. Kendler KS, Aggen SH, Knudsen GP, Roysamb E, Neale MC, Reichborn-Kjennerud T. The structure of genetic and environmental risk factors for syndromal and sub-syndromal common DSM-IV axis I and all axis II disorders. American Journal of Psychiatry. doi: 10.1176/appi.ajp.2010.10030340. (in press) [DOI] [PMC free article] [PubMed] [Google Scholar]
  50. Kendler KS, Myers J, Torgersen S, Neale MC, Reichborn-Kjennerud T. The heritability of cluster A personality disorders assessed by both personal interview and questionnaire. Psychological Medicine. 2008;37:655–665. doi: 10.1017/S0033291706009755. [DOI] [PubMed] [Google Scholar]
  51. Kernberg O. The treatment of patients with borderline personality organization. International Journal of Psychoanalysis. 1968;49:600–619. [PubMed] [Google Scholar]
  52. Kernberg O. Borderline conditions and pathological narcissism. New York: Jason Aronson; 1975. [Google Scholar]
  53. Kernberg OF, Michaels R. Borderline personality disorder. American Journal of Psychiatry. 2009;166:505–508. doi: 10.1176/appi.ajp.2009.09020263. [DOI] [PubMed] [Google Scholar]
  54. King-Casas B, Sharp C, Lomax-Bream L, Lohrenz T, Fonagy P, Montague PR. The rupture and repair of cooperation in borderline personality disorder. Science. 2008;321:806–810. doi: 10.1126/science.1156902. [DOI] [PMC free article] [PubMed] [Google Scholar]
  55. Klonsky D. What is emptiness? Clarifying the seventh criterion for borderline personality disorder. Journal of Personality Disorders. 2008;22:418–426. doi: 10.1521/pedi.2008.22.4.418. [DOI] [PubMed] [Google Scholar]
  56. Koenigsberg HW, Fan J, Ochsner KN, Guise KG, Pizzarello S, Dorantes C, et al. Neural correlates of the use of psychological distancing to regulate responses to negative social cues: A study of patients with borderline personality disorder. Biological Psychiatry. 2009;66:854–863. doi: 10.1016/j.biopsych.2009.06.010. [DOI] [PMC free article] [PubMed] [Google Scholar]
  57. Koenigsberg HW, Harvey PD, Mitropoulou V, Schmeidler J, New AS, Goodman M, et al. Characterizing affective instability in borderline personality disorder. American Journal of Psychiatry. 2002;159:784–788. doi: 10.1176/appi.ajp.159.5.784. [DOI] [PubMed] [Google Scholar]
  58. Korzekwa MI, Dell PF, Links PS, Thabanc L, Fougere P. Dissociation in borderline personality disorder: A detailed look. Journal of Trauma Dissociation. 2010;10:346–367. doi: 10.1080/15299730902956838. [DOI] [PubMed] [Google Scholar]
  59. Krueger RF, Eaton NR. Personality traits and the classification of mental disorders: Toward a more complete integration in DSM-V and an empirical model of psychopathology. Personality Disorders: Theory, Research, and Treatment. doi: 10.1037/a0018990. (in press) [DOI] [PubMed] [Google Scholar]
  60. Kuo JR, Linehan MM. Disentangling emotion processes in border-line personality disorder: Physiological and self-reported assessment of biological vulnerability, baseline intensity, and reactivity to emotionally evocative stimuli. J Abnorm Psychol. 2009;118:531–544. doi: 10.1037/a0016392. [DOI] [PMC free article] [PubMed] [Google Scholar]
  61. Lenzenweger MF, Lane MC, Loranger AW, Kessler RC. DSM-IV personality disorders in the national comorbidity survey replication. Biol Psychiatry. 2007;62:553–564. doi: 10.1016/j.biopsych.2006.09.019. [DOI] [PMC free article] [PubMed] [Google Scholar]
  62. Linehan MM. Dialectical behavioral therapy of borderline personality disorder. New York: Guilford; 1993. [Google Scholar]
  63. Lieb K, Vollm B, Rucker G, Timmer A, Stoffers JM. Pharmacotherapy for borderline personality disorder: Cochrane systematic of randomised trials. British Journal of Psychiatry. 2010;196:4–12. doi: 10.1192/bjp.bp.108.062984. [DOI] [PubMed] [Google Scholar]
  64. Livesley WJ, Jackson DN, Schroeder ML. Factorial structure of traits delineating PDs in clinical and general population samples. Journal of Abnormal Psychology. 1992;101:432–440. doi: 10.1037//0021-843x.101.3.432. [DOI] [PubMed] [Google Scholar]
  65. Lyons-Ruth K, Melnick S, Patrick M, Hobson RP. A controlled study of hostile-helpless states of mind among borderline and dysthymic women. Attachment and Human Development. 2007;3:1–16. doi: 10.1080/14616730601151417. [DOI] [PMC free article] [PubMed] [Google Scholar]
  66. Lynch TR, Chapman AL, Rosenthal MZ, Kuo JR, Linehan MM. Mechanisms of change in dialectical behavior therapy: Theoretical and empirical observations. Journal of Clinical Psychology. 2006;62:459–480. doi: 10.1002/jclp.20243. [DOI] [PubMed] [Google Scholar]
  67. Masterson J. Treatment of the borderline adolescent: A developmental approach. New York: John Wiley & Sons; 1972. [Google Scholar]
  68. Meyer B, Pilkonis PA, Proietti JM, Heape CL, Egan M. Attachment styles and personality disorders as predictors of symptom course. Journal of Personality Disorders. 2001;15:371–389. doi: 10.1521/pedi.15.5.371.19200. [DOI] [PubMed] [Google Scholar]
  69. Morey LC, Shea MT, Markowitz JC, Stout RL, Hopwood CJ, Gunderson JG, et al. State effects of major depression on the assessment of personality and personality disorder. American Journal of Psychiatry. 2010;167:528–535. doi: 10.1176/appi.ajp.2009.09071023. [DOI] [PMC free article] [PubMed] [Google Scholar]
  70. Morse JQ, Hill J, Pilkonis PA, Yaggi K, Broyden N, Stepp S, Reed LI, Feske U. Anger, preoccupied attachment, and domain disorganization in borderline personality disorder. Journal of Personality Disorders. 2009;23:240–257. doi: 10.1521/pedi.2009.23.3.240. [DOI] [PMC free article] [PubMed] [Google Scholar]
  71. New AS, Triebwasser J, Charney DS. The case for shifting borderline personality disorder to axis 1. Biological Psychiatry. 2008;64:653–659. doi: 10.1016/j.biopsych.2008.04.020. [DOI] [PubMed] [Google Scholar]
  72. Nica EI, Links PS. Affective instability in borderline personality disorder: Experience sampling findings. Current Psychiatry Reports. 2009;11:74–81. doi: 10.1007/s11920-009-0012-2. [DOI] [PubMed] [Google Scholar]
  73. Oldham J. Borderline personality disorder comes of age. American Journal of Psychiatry. 2009;166:509–511. doi: 10.1176/appi.ajp.2009.09020262. [DOI] [PubMed] [Google Scholar]
  74. Paris J. The nature of borderline personality disorder: Multiple dimensions, multiple symptoms, but one category. Journal of Personality Disorders. 2007;21:457–473. doi: 10.1521/pedi.2007.21.5.457. [DOI] [PubMed] [Google Scholar]
  75. Regier DA, Narrow WE, Kuhl WE, Kupfer DJ. The conceptual development of DSM-V. American Journal of Psychiatry. 2009;166:645–650. doi: 10.1176/appi.ajp.2009.09020279. [DOI] [PubMed] [Google Scholar]
  76. Reich J. DSM-III personality disorders and the outcome of treated panic disorder. American Journal of Psychiatry. 1988;145:1149–1152. doi: 10.1176/ajp.145.9.1149. [DOI] [PubMed] [Google Scholar]
  77. Rothschild L, Cleland C, Haslam N, Zimmerman M. A taxometric study of borderline personality disorder. Journal of Abnormal Psychology. 2003;112:657–666. doi: 10.1037/0021-843X.112.4.657. [DOI] [PubMed] [Google Scholar]
  78. Sanislow CA, Grilo CM, Morey LC, Bender DS, Skodol AE, Gunderson JG, et al. Confirmatory factor analysis of DSM-IV criteria for borderline personality disorder: Findings from the collaborative longitudinal personality disorders study. American Journal of Psychiatry. 2002;159:284–290. doi: 10.1176/appi.ajp.159.2.284. [DOI] [PubMed] [Google Scholar]
  79. Scott LN, Levy KN, Pincus AL. Adult attachment, personality traits, and borderline personality disorder features in young adults. Journal of Personality Disorders. 2009;23:258–228. doi: 10.1521/pedi.2009.23.3.258. [DOI] [PMC free article] [PubMed] [Google Scholar]
  80. Shanks C, Pfohl B, Blum N, Black DW. Can negative attitudes toward patients with borderline personality disorder be changed? The effect of attending a STEPPES work shop. Journal of Personality Disorders. doi: 10.1521/pedi.2011.25.6.806. (in press) [DOI] [PubMed] [Google Scholar]
  81. Shedler J, Beck A, Fonagy P, Gabbard GO, Gunderson JG, Kernberg O, Michels R, Westen D. Commentary for American Journal of Psychiatry Personality Disorders in DSM-5. 2010;167:1026–1028. doi: 10.1176/appi.ajp.2010.10050746. [DOI] [PubMed] [Google Scholar]
  82. Shedler J, Westen D. Refining personality disorder diagnosis: Integrating science and practice. American Journal of Psychiatry. 2004;161:1350–1365. doi: 10.1176/appi.ajp.161.8.1350. [DOI] [PubMed] [Google Scholar]
  83. Siever LJ, Torgerson S, Gunderson JG, Livesley WJ, Kendler KS. The borderline diagnosis III: Identifying endophenotypes for genetic studies. Biological Psychiatry. 2002;51:964–968. doi: 10.1016/s0006-3223(02)01326-4. [DOI] [PubMed] [Google Scholar]
  84. Silverman JM, Pinkham L, Horvath TB, Coccaro EF, Klar H, Schear S, et al. Affective and impulsive personality disorder traits in the relatives of patients with borderline personality disorder. American Journal of Psychiatry. 1991;148:1378–1385. doi: 10.1176/ajp.148.10.1378. [DOI] [PubMed] [Google Scholar]
  85. Skodol AE, Gunderson JG, Pfohl B, Widiger TA, Livesley WJ, Siever L. The borderline diagnosis I: Psychopathology, comorbidity, and personality structure. Biological Psychiatry. 2002;51:936–950. doi: 10.1016/s0006-3223(02)01324-0. [DOI] [PubMed] [Google Scholar]
  86. Skodol AE, Pagano ME, Bender DS, Shea MT, Gunderson JG, Yen S, et al. Stability of functional impairment in patients with schizotypal, borderline, avoidant, or obsessive-compulsive personality disorder over two years. Psychological Medicine. 2004;35:443–451. doi: 10.1017/s003329170400354x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  87. Spitzer RL, Endicott J, Gibbon M. Crossing the border into borderline personality and borderline schizophrenia: The development of criteria. Archives of General Psychiatry. 1979;36:17–24. doi: 10.1001/archpsyc.1979.01780010023001. [DOI] [PubMed] [Google Scholar]
  88. Stanley B, Siever LJ. The interpersonal dimension of borderline personality disorder: Toward a neuro-peptide model. American Journal of Psychiatry. 2010;167:24–39. doi: 10.1176/appi.ajp.2009.09050744. [DOI] [PMC free article] [PubMed] [Google Scholar]
  89. Sternbach SE, Judd PH, Sabo AN. Cognitive and perceptual distortions in borderline personality disorder and schizotypal personality disorder in a vignette sample. Comprehensive Psychiatry. 1992;33:186–189. doi: 10.1016/0010-440x(92)90028-o. [DOI] [PubMed] [Google Scholar]
  90. Stiglmayr CE, Ebner-Priemer UW, Bretz J, Behm R, Mohse M, Lammers CH, et al. Dissociative symptoms are positively related to stress in borderline personality disorder. Acta Psychiatrica Scandinavica. 2008;117:139–147. doi: 10.1111/j.1600-0447.2007.01126.x. [DOI] [PubMed] [Google Scholar]
  91. Stiglmayr CE, Grathwoll T, Linehan MM, Ihorst G, Fahrenberg J, Bohus M. Aversive tension in patients with borderline personality disorder: A computer-based controlled field study. Acta Psychiatrica Scandinavica. 2005;3:372–379. doi: 10.1111/j.1600-0447.2004.00466.x. [DOI] [PubMed] [Google Scholar]
  92. Stiglmayr C, Shapiro DA, Stieglitz RD, Limberger M, Bohus M. Experience of aversive tension and dissociation in female patients with borderline personality disorder—A controlled study. Journal of Psychiatric Research. 2001;35:111–118. doi: 10.1016/s0022-3956(01)00012-7. [DOI] [PubMed] [Google Scholar]
  93. Torgersen S, Czajkowski N, Jacobson K, Reichborn-Kjennerud T, Roysamb E, Neale MC, Kendler KS. Dimensioanl representation of DSM-IV cluster B personality disorders in a population-based sample of Norwegian twins: A multivariate study. Psychol Med. 2008;11:1617–1625. doi: 10.1017/S0033291708002924. [DOI] [PubMed] [Google Scholar]
  94. Torgersen S, Lygren S, Øien PA, Skre I, Onstad S, Edvardsen J, Tambs K, Kringlen E. A twin study of personality disorders. Comprehensive Psychiatry. 2000;41:416–425. doi: 10.1053/comp.2000.16560. [DOI] [PubMed] [Google Scholar]
  95. Trull TJ, Jahng S, Tomko RL, Wood PK, Sher KJ. Revised NESARC personality disorder diagnoses: Gender, prevalence, and comorbidity with substance dependence disorders. Journal of Personality. 2010;24:412–426. doi: 10.1521/pedi.2010.24.4.412. [DOI] [PMC free article] [PubMed] [Google Scholar]
  96. Trull TJ, Solhan MB, Tragesser SL, Jahng S, Wood PK, Piasecki TM, Watson D. Affective instability: Measuring a core feature of borderline personality disorder with ecological momentary assessment. Journal of Abnormal Psychology. 2008;117:647–661. doi: 10.1037/a0012532. [DOI] [PubMed] [Google Scholar]
  97. Unoka Z, Seresm I, Aspan N, Bodi N, Keri S. Trust game reveals restricted interpersonal transactions in patients with borderline personality disorder. Journal of Personality Disorders. 2009;23:399–409. doi: 10.1521/pedi.2009.23.4.399. [DOI] [PubMed] [Google Scholar]
  98. Wagner AW, Linehan MM. Facial expression recognition ability among women with borderline personality disorder: Implications for emotion regulation. Journal of Personality Disorders. 1999;13:329–344. doi: 10.1521/pedi.1999.13.4.329. [DOI] [PubMed] [Google Scholar]
  99. Waller NG, Ross CA. The prevalence and biometric structure of pathological dissociation in the general population: Taxometric and behavior genetic findings. Journal of Abnormal Psychology. 1997;106:99–110. doi: 10.1037//0021-843x.106.4.499. [DOI] [PubMed] [Google Scholar]
  100. Walter M, Gunderson JG, Zanarini MC, Sanislow CA, Morey LC, Yen S, Skodol AE, Stout RL. New onsets of substance use disorders in borderline personality disorder over 7 years of follow-ups: Findings from the collaborative longitudinal personality disorder study. Addiction. 2009;104:97–103. doi: 10.1111/j.1360-0443.2008.02413.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  101. Westen D, Shedler J. Revising and assessing axis II, part II: Toward an empirically based and clinically useful classification of personality disorders. American Journal of Psychiatry. 1999;156:273–285. doi: 10.1176/ajp.156.2.273. [DOI] [PubMed] [Google Scholar]
  102. White CN, Gunderson JG, Zanarini MC, Hudson JI. Family studies of borderline personality disorder: A review. Harvard Review of Psychiatry. 2003;11:8–19. doi: 10.1080/10673220303937. [DOI] [PubMed] [Google Scholar]
  103. Winograd G, Cohen P, Chen H. Adolescent borderline symptoms in the community: Prognosis for functioning over 20 years. J Assoc Child Adol Ment Res. 2008;49:933–941. doi: 10.1111/j.1469-7610.2008.01930.x. [DOI] [PubMed] [Google Scholar]
  104. Woody GE, McLellan T, Luborsky L, O’Brien C. Sociopathy and psychotherapy outcome. Archives of General Psychiatry. 1985;42:1081–1086. doi: 10.1001/archpsyc.1985.01790340059009. [DOI] [PubMed] [Google Scholar]
  105. Yen S, Shea MT, Battle CL, Johnson DM, Zlotnick C, Dolan-Sewell R, et al. Traumatic exposure and posttraumatic stress disorder in borderline, schizotypal, avoidant, and obsessive-compulsive personality disders: Findings from the collaborative longitudinal personality disorders study. Journal of Nervous and Mental Disorders. 2002;190:510–518. doi: 10.1097/00005053-200208000-00003. [DOI] [PubMed] [Google Scholar]
  106. Young JE, Klosko J, Weishaar ME. Schema therapy: A practitioner’s guide. New York: Guilford Press; 2003. [Google Scholar]
  107. Zanarini MC, Frankenburg FR, DeLuca CJ, Henen J, Khera GS, Gunderson JG. The pain of being borderline: Dysphoric states specific to borderline personality disorder. Harvard Review of Psychiatry. 1998;6:201–207. doi: 10.3109/10673229809000330. [DOI] [PubMed] [Google Scholar]
  108. Zanarini MC, Frankenburg FR, Reich DB, Fitzmaurice G. The 10-year course of psychosocial functioning among patients with borderline personality disorder and axis II comparison subjects. Acta Psychiatrica Scandinavica. 2010;122:103–109. doi: 10.1111/j.1600-0447.2010.01543.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  109. Zanarini MC, Frankenburg FR, Reich DB, Fitzmaurice G, Weinberg I, Gunderson JG. The 10-year course of physically self-destructive acts reported by borderline patients and axis II comparison subjects. Acta Psychiatrica Scandinavica. 2008;117:177–184. doi: 10.1111/j.1600-0447.2008.01155.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  110. Zanarini MC, Frankenburg FR, Reich DB, Silk KR, Hudson JL, McSweeney LB. The subsyndromal phenomenology of borderline personality disorder: A 10-year follow up study. American Journal of Psychiatry. 2007;164:920–935. doi: 10.1176/ajp.2007.164.6.929. [DOI] [PubMed] [Google Scholar]
  111. Zanarini MC, Frankenburg FR, Yong L, Raviola G, Reich DB, Hennen J, Hudson JI, Gunderson JG. Borderline psychopathology in the first-degree relatives of borderline and axis II comparison probands. Journal of Personality Disorders. 2004;18:439–447. doi: 10.1521/pedi.18.5.439.51327. [DOI] [PubMed] [Google Scholar]
  112. Zanarini MC, Hudson J, Choi-Kain LW, Gunderson JG. Familiality of BPD. Presented at the 162nd Annual meeting of the American Psychiatric Association; San Francisco, CA. 2009. May, [Google Scholar]
  113. Ziegler-Hill V, Abraham J. Borderline personality features: Instability of self-esteem and affect. J Soc Clin Psychol. 2006;25:668–687. [Google Scholar]
  114. Zimmerman M, Mattia J. Axis I diagnostic comorbidity and borderline personality disorder. Comprehensive Psychiatry. 1999;40:245–252. doi: 10.1016/s0010-440x(99)90123-2. [DOI] [PubMed] [Google Scholar]
  115. Zimmerman M, Coryell W. DSM-III personality disorder diagnoses in a nonpatient sample. Demographic correlates and comorbidity. Archives of General Psychiatry. 1989;46:262–269. doi: 10.1001/archpsyc.1989.01810080012002. [DOI] [PubMed] [Google Scholar]
  116. Zimmerman M, Ruggero CJ, Chelminski I, Young D. Psychiatric diagnoses in patients previously diagnosed with bipolar disorder. Journal of Clinical Psychiatry. 2010;71:26–31. doi: 10.4088/JCP.08m04633. [DOI] [PubMed] [Google Scholar]

RESOURCES